The effects of a respiratory acidosis on human heart rate variability

Human heart rate variability (HRV) was examined during a mild respiratory acidosis induced by inhalation of a normoxic hypercapnic gas mixture. On two separate occasions, separated by 72 but not more than 120hr, ECG was recorded from 9 normotensive subjects during supine rest. ECG was recorded for 20 min breathing room air or a 5% CO2 in normoxic air mixture. Expired V'E, O2 and CO2 were measured with breath-by-breath mass spectrometry. HRV spectra were calculated using a Welch averaged periodogram method and banded as Very Low Frequency (VLF: 0 - 0.04 Hz), Low Frequency (LF: 0.04 - 0.15 Hz), and High Frequency (HF: 0.15 - 0.4Hz). Student paired samples t-tests were used to compare room air (RA) versus inhaled 5% CO2 in air (5% CO2) data. All results reported as mean +/- SD. In the HRV time domain, hypercapnic normoxia reduced mean r-r intervals (5% CO2: 956.1 +/- 149.2 vs. RA: 1035 +/- 146.8 ms, p = 0.022) and median r-r intervals (5% CO2: 942.6 +/- 153.1 vs. RA: 1047.8 +/- 157.3 ms, p = 0.010), and increased heart rates (5% CO2: 64.4 +/- 12 vs. RA: 59.3 +/- 10.1 bpm, p = 0.019). In the HRV frequency domain, hypercapnic normoxia increased the high frequency component of HRV (5% CO2: 9799 +/- 7649 vs. RA: 4399 +/- 3857 ms2, p = 0.004) and reduced the LF/HF ratio (5% CO2: 0.243 +/- 0.145 vs. RA: 0.906 +/- 0.672, p = 0.017). An incomplete ventilatory compensation probably accounts for the increased HF contribution. An increased heart rate with a mild respiratory acidosis may be caused by a vasodilator effect of elevated arterial PCO2, stimulating the increase in heart rate to maintain blood pressure.